Prophylactic anticoagulation: comment on the American College of Rheumatology Guidance for Management of Multisystem Inflammatory Syndrome in Children

In December 2019, China reported cases of infections caused by a new zoonotic coronavirus, which gradually developed into a pandemic. The disease was initially believed to be mild in children. In April 2020, a possible relationship between a new paediatric multisystem inflammatory syndrome and SARS-CoV-2 was found. In May, the Royal College of Paediatrics and Child Health published the criteria for the diagnosis of this new disease. We present a case of a 6-year-old boy retrospectively diagnosed with SARS-CoV-2-related multisystem inflammatory syndrome based on medical history, physical examination, laboratory and imaging findings, as well as the available literature.

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TRENDY DIAGNOSIS OF «AUTO-INFLAMMATORY SYNDROME»: WHAT IS BEHIND THIS?

PEDIATRIA Journal named after G N SPERANSKY ◽

10.24110/0031-403x-2019-98-3-145-150 ◽

2019 ◽

Vol 98 (3) ◽

pp. 145-150

Author(s):

S.O. Salugina ◽

◽

E.S. Fedorov ◽

Keyword(s):

Inflammatory Syndrome

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COVID-19 in children: Pathogenesis and current status

Allergy and Asthma Proceedings ◽

10.2500/aap.2020.42.200104 ◽

2020 ◽

Author(s):

Lawrence Frenkel ◽

Fernando Gomez ◽

Joseph A Bellanti

Keyword(s):

Respiratory Disease ◽

Respiratory Symptoms ◽

Distress Syndrome ◽

Clinical Course ◽

Current Status ◽

Current Evidence ◽

Initial Description ◽

Relationship Of ◽

Inflammatory Syndrome ◽

The Relationship

Background: Since its initial description in December 2019 in Wuhan, China, coronavirus disease 2019 (COVID-19) has rapidly progressed into a worldwide pandemic, which has affected millions of lives. Unlike the disease in adults, the vast majority of children with COVID-19 have mild symptoms and are largely spared from severe respiratory disease. However, thereare children who have significant respiratory disease, and some may develop a hyperinflammatory response similar to thatseen in adults with COVID-19 and in children with Kawasaki disease (KD), which has been termed multisystem inflammatory syndrome in children (MIS-C).Objective: The purpose of this report was to examine the current evidence that supports the etiopathogenesis of COVID-19 in children and the relationship of COVID-19 with KD and MIS-C as a basis for a better understanding of the clinical course, diagnosis, and management of these clinically perplexing conditions.Results: The pathogenesis of COVID-19 is carried out in two distinct but overlapping phases of COVID-19: the first triggered by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) itself and the second by the host immune response. Children with KD have fewer of the previously described COVID-19–associated KD features with less prominent acute respiratory distress syndrome and shock than children with MIS-C.Conclusion: COVID-19 in adults usually includes severe respiratory symptoms and pathology, with a high mortality. Ithas become apparent that children are infected as easily as adults but are more often asymptomatic and have milder diseasebecause of their immature immune systems. Although children are largely spared from severe respiratory disease, they canpresent with a SARS-CoV-2–associated MIS-C similar to KD.

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Correlation Between Serological Makers and Immunofluorescence Deposits i n Kidney Tissue of Patients with Lupus Nephritis

International Journal of Drug Delivery Technology ◽

10.25258/ijddt.9.2.22 ◽

2019 ◽

Vol 9 (02) ◽

Author(s):

Haider S Al-Hadad ◽

Aqeel Abbas Matrood ◽

Maha Abdalrasool Almukhtar ◽

Haider Jabur Kehiosh ◽

Riyadh Muhi Al-Saegh

Keyword(s):

Lupus Nephritis ◽

Lupus Erythematosus ◽

Kidney Biopsy ◽

Pearson Correlation ◽

Standard Procedure ◽

Kidney Tissue ◽

P Value ◽

American College Of Rheumatology ◽

Immune Deposits ◽

Number Of Patients

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease. Few biomarkers for SLE have been validated and widely accepted for the laboratory follow-up of inflammatory activity. In SLE patients, with lupus nephritis (LN), complement activation leads to fluctuation of serum C3 and C4 that are frequently used as clinicalm biomarker of disease activity in SLE. Patients and Methods: In this study the number of patients were 37, seven patients were excluded for incomplete data collection, 28 were females ,2 were males. The duration of the study is two years from 2015 to 2017. Patients were considered to have SLE and LN according to American College of Rheumatology (ACR) criteria, and International Society of Nephrology/ Renal Pathology Society (ISN/RPS). All patients were evaluated withm clinical presentation, laboratory investigations. Our patients underwent kidney biopsy according to standard procedure by Kerstin Amann, and their tissue specimens were studied in the laboratory with light microscope (LM) and immunofluorescence microscope reagents. The relationship between the serological markers and immunofluorescence deposits in kidney biopsy of all patients were studied using the statistical analysis of Pearson correlation and single table student's T test. A P value 0.05 was considered statistically significant. Results: The granular pattern of IF deposits was present in all LN patients, and in more than two third of patients these IF deposits presented in glomerular, tubular, and mesangium sites. While less than one third of patients had IF deposits in the mesangium only. There was no statistically significant correlation between serum ANA, anti-dsDNA, and IF deposits of different types. There was significant correlation between serum C3 and C4 hypocomplementemia and IgG immune deposits in kidney biopsy, and there was significant relationship between serum C3 hypocomplementemia and full house immunofluorescence (FHIF) deposits inm kidney biopsy.Conclusions:Immunofluorescence deposits is mainly granular pattern in LN patients. There was no significant association between serum ANA, anti-dsDNA, and immune deposits in kidney tissue. Immunofluorescence deposits of IgG type correlates significantly with serum C3 and C4 hypocomplemetemia, and these immune deposits in association with low complement levels correlates with LN flare. There was significant correlation between C3 hypocomplementemia and FHIF.

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